Abstract
Background/Objectives
Empirical data consistently suggest high heritability estimates for adiposity, with heritability peaking during childhood. However, no study has considered the potentially shared genetic and environmental etiologies of the three most commonly used adiposity metrics — body mass index (BMI), waist circumference, and percent body fat. We examined the genetic and environmental contributions to BMI, percent body fat, and waist circumference, and the extent to which their genetic and environmental variances overlap during middle childhood.
Subjects/Methods
We examined the genetic and environmental contributions to BMI, percent body fat, and waist circumference in a community sample of twin children (N = 254–326 pairs; female=47.8–49.9%; Non-Hispanic White=51.9–59.5%, Hispanic=29.5–35.7%) studied at ages 8, 9, 10, and 11 years by comparing the fit of two models: the independent and common pathway models.
Results
The common pathway model yielded the most parsimonious fit, indicating that covariance between indicators was best represented by a single highly heritable common latent factor. This common factor explained 97-98% of the variance in BMI regardless of age, whereas indicator-specific genetic and environmental influences explained 10–17% of the variance in percent body fat and 14–29% of the variance in waist circumference.
Conclusions
Our findings support a highly heritable common adiposity factor for BMI, body fat, and waist circumference in a community sample of youth, and suggest that BMI is a useful measure of adiposity in large-scale epidemiological studies with limited resources in middle childhood. When resources permit, including other adiposity indicators such as percent body fat and waist circumference can provide more precise assessments for specific subgroups. Our study highlights the need for individualized approaches to managing childhood adiposity, recognizing the strong genetic component and the variability in how children respond to their environments. Theories of the etiology of childhood obesity should accommodate genetic influences to optimize prevention and intervention efforts.
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Data availability
The datasets generated during and/or analyzed during the current study are available from the corresponding author upon reasonable request.
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Acknowledgements
We acknowledge support from the National Institutes of Health for funding this research (2R01 HD086085: MPI’s Kathryn Lemery-Chalfant & Mary Davis; 2R01 HD079520-06; MPI’s Kathryn Lemery-Chalfant and Leah Doane). We also thank the Arizona Twin Project students and staff and families, and the participating twins and families.
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All authors contributed to the study conception and design. Data analyses were performed by EB and SC. EB conceptualized the research questions and hypotheses, interpreted results, and drafted the manuscript. SC, MD, LD, and KL contributed to the interpretation of the data, revised the manuscript critically for important intellectual content, and gave final approval of the version to be published.
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Arizona State University Institutional Review Board approval was obtained for all study phases prior to data collection for each phase of this study (IRB# STUDY00000637- Children’s Sleep and Health and STUDY00004309- Children’s Pain). All methods were performed in accordance with the relevant guidelines and regulations provided by the IRB. Written informed consent was provided by the participants’ primary caregivers, and verbal assent was given by twin children prior to assessments at each wave of data collection.
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Bartsch, E.M., Clifford, S., Davis, M.C. et al. Does a heritable common latent factor explain body mass index, percent body fat, and waist circumference across childhood?. Int J Obes (2025). https://doi.org/10.1038/s41366-025-01864-9
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DOI: https://doi.org/10.1038/s41366-025-01864-9